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These data provide the first evidence for a physiologic role of these isoforms in RET pathway function.
Significantly, we show that introduction of mapk10 (show MAPK10 Proteins) mutations into ret heterozygotes enhanced the ENS deficit, supporting MAPK10 (show MAPK10 Proteins) as a Hirschsprung disease (HSCR (show EDNRB Proteins)) susceptibility locus. Our studies demonstrate that ret heterozygous zebrafish is a sensitized model, with many significant advantages over existing murine models, to explore the pathophysiology and complex genetics of HSCR (show EDNRB Proteins).
RET expression is investigated within the brain of zebrafish; both RET protein and mRNA are observed.
In animals lacking Ret or Gfra3 (show GFRA3 Proteins) function, myogenic gene expression is reduced in forming opercular muscles, but not in non-opercular muscles derived from the same muscle anlagen.
evaluation of noncoding sequences at the zebrafish ret locus conserved among teleosts, and at the human RET locus, conserved among mammals
genes beyond RET may be implicated in the genesis of sporadic cases of HD
These results implicate EGFR (show EGFR Proteins) as a key regulator of RET activation in A+AD and suggest that EGFR (show EGFR Proteins) inhibitors may be therapeutic in patients with A+AD tumors even in the absence of an EGFR (show EGFR Proteins) or RET mutation.
In a cohort of MEN 2 families, the distribution of RET mutations in Denmark appears to differ from that of other populations. Mutations in codon 611 were the most prevalent, followed by more frequently reported mutations. This might be due to a possible founder effect for the p.C611Y mutation.
RET inhibitors could both impair primary tumor growth and tumor dissemination, thereby providing a potential therapeutic advantage when used in combination with aromatase (show CYP19A1 Proteins) inhibitors in postmenopausal ER+ breast cancers.
exposure of medullary thyroid cancer cells to a tri (show VANGL2 Proteins)-substituted naphthalene diimide resulted in a significant antiproliferative activity paralleled by inhibition of RET expression
Our data show that RET expression promotes a more mesenchymal phenotype with reduced cell-cell adhesion and increased invasiveness in papillary thyroid carcinoma cell models, but is more important for tumour cell survival, proliferation and anoikis resistance in medullary thyroid carcinoma models. Our data suggest that the RET51 isoform plays a more prominent role in mediating these processes compared to RET9.
From this case series, the largest such experience to date, it is concluded that the RET(K666N) variant is likely pathogenic and associated with low penetrance of medullary thyroid carcinoma.
Multilayer OMIC data analysis uncovered methylation hallmarks in genetically defined Medullary thyroid carcinoma (MTC (show MT1A Proteins)) and revealed JAK (show JAK3 Proteins)/Stat (show STAT1 Proteins) signaling effector STAT3 (show STAT3 Proteins) as a potential therapeutic target for the treatment of RET(M918T) MTCs
DNA mutational analysis of RET germline mutations associated with medullary thyroid carcinoma in a Druze family.
These data suggest that angiogenesis in RET mutation medullary thyroid carcinomas may be more intense and complete than that found in RETwt tumors, a feature that might increase their susceptibility to antiangiogenic therapy.
Significant genetic risk for Hirschsprung disease (HSCR (show EDNRB Proteins)) was imparted by rs2435357 and rs2506030 at RET and by rs12707682 at SEMA3 in a Chinese population. No evidence was found of a genetic association between HSCR (show EDNRB Proteins) and either of the NRG1 (show NRG1 Proteins) SNPs rs7835688 and rs16879552, at either allele or genotype level.
Compromised Survival of Cerebellar Molecular Layer Interneurons Lacking GDNF Receptors GFRalpha1 (show GFRA1 Proteins) or RET Impairs Normal Cerebellar Motor Learning
Data show that NEDL2 regulates GDNF/Ret/Akt pathway depends on its Nedd8 ligase activity rather than ubiquitin ligase activity.
The cardiac GFRA2 (show GFRA2 Proteins) signaling pathway is distinct from the canonical pathway dependent on the RET tyrosine kinase (show TYRO3 Proteins).
Ret is essential to mediate GDNF's neuroprotective and neuroregenerative effect in a Parkinson disease mouse model.
Mechanistically, Ret is engaged in a positive feedback loop with Wnt/Wingless signalling, modulated by Src and Fak kinases.
Authors did not find evidence for genetic interaction between Ret and Sema3d (show SEMA3D Proteins) affecting survival, presence of myenteric plexus or intestine transcriptome.
findings uncover a novel spinal circuit that mediates crosstalk between touch and pain pathways and suggest that some early RET positive Dorsal Horn neurons could function as pain "gating" neurons.
Using an organ culture system for prostate development and Ret mutant mice, we demonstrate that RET-mediated GDNF signaling in UGS increases proliferation of mesenchyme cells and suppresses androgen-induced proliferation and differentiation of prostate epithelial cells, inhibiting prostate development.
we described a RET-ER81 (show ETV1 Proteins)-Neuregulin1 signaling pathway in neurons innervating Pacinian corpuscle somatosensory end organs, which is essential for communication between the innervating axon and the end organ
This gene, a member of the cadherin superfamily, encodes one of the receptor tyrosine kinases, which are cell-surface molecules that transduce signals for cell growth and differentiation. This gene plays a crucial role in neural crest development, and it can undergo oncogenic activation in vivo and in vitro by cytogenetic rearrangement. Mutations in this gene are associated with the disorders multiple endocrine neoplasia, type IIA, multiple endocrine neoplasia, type IIB, Hirschsprung disease, and medullary thyroid carcinoma. Two transcript variants encoding different isoforms have been found for this gene. Additional transcript variants have been described but their biological validity has not been confirmed.
proto-oncogene tyrosine-protein kinase receptor Ret
, receptor tyrosine kinase
, ret proto-oncogene
, proto-oncogene tyrosine-protein kinase receptor Ret-like
, RET transforming sequence
, cadherin family member 12
, cadherin-related family member 16
, hydroxyaryl-protein kinase
, proto-oncogene c-Ret
, ret proto-oncogene (multiple endocrine neoplasia and medullary thyroid carcinoma 1, Hirschsprung disease)
, Ret gene for receptor tyrosin
, Ret proto-oncogene (multiple endocrine neoplasia MEN2A MEN2B and medullary thyroid carcinoma 1 Hirschsprung disease)
, ret tyrosine kinase